Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Color Doppler sonography (CDS--spectral, color and power), harmonic imaging techniques (THI, PHI), possibility of 3D analysis of picture, usage of contrast agents, have raised the values of ultrasound as a diagnostic method to a very high level. THI--non-linear gray scale modality, is based on the processing of higher reflected frequencies, that has improved a picture resolution, which is presented with less artifacts and limiting effects of obesity and gases. Ultrasound contrast agents improve analysis of micro and macro circulation of the examined area, and with the assessment of velocity of supply in ROI (wash in), distribution and time of signal weakening (wash out), are significantly increasing diagnostic value of ultrasound. Besides the anatomical and topographic presentation of examined region (color, power), Color Doppler sonography gives us haemodynamic-functional information on vascularisation of that region, as well as on pathologic vascularisation if present. Avascular aspect of a focal pathologic lesion corresponds to a cyst or haematoma, while coloration and positive spectral curve discover that anechogenic lesions actually represents aneurysms, pseudoaneurysms or AVF. In local inflammatory lesion, abscess in an acute phase, CDS shows first increased, and then decreased central perfusion, while in a chronic phase, a pericapsular vascularisation is present. Contribution of CDS in differentiation of hepatic tumors (hemangioma, HCC and metastasis) is very significant. Central color dots along the peripheral blood vessels and the blush phenomenon are characteristics of capillary hemangioma, peritumoral vascular ring "basket" of HCC, and "detour" sign of metastasis. The central artery, RI from 0.45 to 0.60 and radial spreading characterize FNH. Hepatic adenoma is characterized by an intratumoral vein, and rarely by a vascular hallo. Further on, blood velocity in tumor defined by Color Doppler, distinguishes malignant from benign lesion, where 40 cm/s is a rough border value. Values of DPI (Doppler perfusion index) over 0.3 and tumor index over 1.0 characterize primary, and lower values characterize secondary liver malignancies. In differentiation of benign and malign tumors of kidneys, besides the aspect of vascularisation, the maximal frequency altitude in tumor artery (the limit around 2.5 kHz) is very important. However, peripheral and penetrating blood vessels are most usually seen in RCC, less often in AML and bigger oncocytomas. CDS with contrast agent is very useful in making differential diagnosis of the focal lesions with 95% specificity for some lesions.
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PMID:[Color Doppler sonography of focal abdominal lesions]. 1513 25

Type Ia Glycogen storage disease is an autosomal recessive hepatic metabolic disease due to a lack of glucose-6-phosphatase (G-6-Pase) activity presenting with growth retardation, lactic acidosis, fasting hypoglycemia with hypoinsulinemia, hyperuricemia, hepatomegaly, and hepatic adenoma with a risk of malignancy. The gene that encodes G-6-Pase was mapped to 17q21. There are some genotype-phenotype correlations. We report a case with delF327 mutation which is devoid of G-6-Pase activity; however clinical presentation in this case differs somewhat. Although correction of hypoglycemia and lactic acidosis with nocturnal intragastric feeding and uncooked starch therapy improves growth failure, mean height of the patients is often less than the target. Normal height and obesity in this case with hepatic steatosis and low hepatic glycogen storage requires clinical reevaluation since there are some overlapping phenotypes between type Ia GSD and metabolic syndrome. The phenomenon may be related to insulin resistance as a consequence of early aggressive nutrition therapy with frequent low glycemic index meals.
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PMID:Obesity and reversed growth retardation in a child with type Ia glycogen storage disease. 2066 51

Rising incidence of hepatocellular carcinoma (HCC) has been noted in recent years along with diabetes for which reasons and mechanisms are unclear. The rise in HCC is attributed to increasing rates of hepatitis C virus (HCV) infections while increases in diabetes are attributed to obesity. Increased HCC risk has also been noted in diabetes and obesity. Cadmium, a common food contaminant and a constituent of cigarette smoke, is one of ten chemicals considered by the World Health Organization to be of major public health concern. A correlation of cadmium intakes and increased HCC mortality risk has been noted in an ecological study while both hepatocellular carcinoma and hepatic adenoma occurred in cadmium-exposed mice. In the U.S. NHANES III, urinary cadmium levels, indicative of long-term exposure, have been associated with pre-diabetes and diabetes in a dose dependent manner. Intriguing possibility is that cadmium may increase HCC risk through increasing the frequency of hepatogenous diabetes. Overall aim of the present review is to explore if cadmium is a relevant risk factor in chronic liver disease and a rising HCC incidence. It will highlight cadmium levels detectable in various foods, livers, kidneys and urine samples of humans together with global health threat of ingested cadmium, pointing to measures for reducing exposure and a need for revision of guidelines for safe intake levels. Lastly, it will examine evidence for potential roles of cadmium in chronic liver diseases and HCC risk in a call for human case-control studies and animal experiments to elucidate underlying molecular mechanisms.
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PMID:Long-term exposure to cadmium in food and cigarette smoke, liver effects and hepatocellular carcinoma. 2245 52

Growth hormone has been known to be diabetogenic for almost a century and it's diabetogenic properties fostered consideration of excessive and abnormal GH secretion as a cause of diabetes, as well as a role in the microvascular complications, especially retinopathy. However, besides inducing insulin resistance, GH also is lipolytic and a major anabolic hormone for nitrogen retention and protein synthesis. These actions are best illustrated at the extremes of GH secretion: Gigantism/acromegaly is characterized by excessive growth, CHO intolerance, hyperplasia of bone, little body fat and prominent muscle development, whereas total deficiency of GH secretion or action is associated with adiposity, poor growth, and poor muscle development. These actions also become apparent during puberty and pregnancy, times when GH secretion is increased and account for the characteristic changes in body composition and tendency to diabetes. More recently, tissue specific deletions of the GH receptor (GHR), have uncovered newer metabolic effects including it's essential role in triglyceride export from the liver when GHR is deleted in the liver, leading to hepatic steatosis and ultimately to hepatic adenoma formation, effects which may explain these findings in obesity, a state of diminished GH secretion and action. In addition deletion of GH action in muscle and fat is associated with specific patterns of disturbed phenotype and metabolic effects in CHO, fat, and protein metabolism affecting the specific tissue and whole body function. This chapter provides an overview of these classic and newer metabolic functions of GH, placing this hormone and its actions in a central role of body fuel economy in health and disease.
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PMID:Traditional and novel aspects of the metabolic actions of growth hormone. 2619 64